The pathogenetic cascade of meconium aspiration syndrome (MAS) in newborn infants is complex and still incompletely studied. The variable clinical presentation of MAS is basically connected with variation of the amount and consistency of aspirated meconium and also its distribution within the affected lungs. The contributing role of other factors, like intrauterine fetal compromises, lung maturity at the time of insult as well as direct and indirect effects of meconium and its components on the lung alveolar and vascular integrity and development, remains to be studied in further detail. Better understanding of the lung injury processes in MAS, specifically inflammatory injury and non-inflammatory apoptosis and their interplay, may offer new possibilities to treat the severely affected infants, and needs therefore to be explored. Systemic dispersion of intrapulmonary meconium and its components may further induce inflammatory circulatory changes and injurious effects in distant organs, but the mechanisms and clinical significance of these systemic complications are still poorly known. It is thus evident that lung injury processes and potent long-term consequences in various extrapulmonary organs, specifically the brain, as well as development of new approaches to their treatment and prevention form great challenges for future research of MAS.
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